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Titolo:
Reduced antinociception and plasma extravasation in mice lacking a neuropeptide Y receptor
Autore:
Naveilhan, P; Hassani, H; Lucas, G; Blakeman, KH; Hao, JX; Xu, XJ; Wiesenfeld-Hallin, Z; Thoren, P; Ernfors, P;
Indirizzi:
Karolinska Inst, Dept Med Biochem & Biophys, Mol Neurobiol Lab, S-17177 Stockholm, Sweden Karolinska Inst Stockholm Sweden S-17177 Lab, S-17177 Stockholm, Sweden Karolinska Inst, Dept Physiol & Pharmacol, S-17177 Stockholm, Sweden Karolinska Inst Stockholm Sweden S-17177 acol, S-17177 Stockholm, Sweden Karolinska Inst, Huddinge Univ Hosp, Div Clin Neurophysiol, Dept Med Lab Sci & Technol, S-14186 Huddinge, Sweden Karolinska Inst Huddinge Sweden S-14186 echnol, S-14186 Huddinge, Sweden
Titolo Testata:
NATURE
fascicolo: 6819, volume: 409, anno: 2001,
pagine: 513 - 517
SICI:
0028-0836(20010125)409:6819<513:RAAPEI>2.0.ZU;2-O
Fonte:
ISI
Lingua:
ENG
Soggetto:
STRESS-INDUCED ANALGESIA; SCIATIC-NERVE INJURY; SUBSTANCE-P; PERIPHERAL AXOTOMY; NEUROPATHIC PAIN; FEEDING-BEHAVIOR; SPINAL-CORD; RAT; NEURONS; COMPLEMENTARY;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Agriculture,Biology & Environmental Sciences
Life Sciences
Physical, Chemical & Earth Sciences
Citazioni:
30
Recensione:
Indirizzi per estratti:
Indirizzo: Ernfors, P Karolinska Inst, Dept Med Biochem & Biophys, Mol Neurobiol Lab,S-17177 Stockholm, Sweden Karolinska Inst Stockholm Sweden S-17177 77 Stockholm, Sweden
Citazione:
P. Naveilhan et al., "Reduced antinociception and plasma extravasation in mice lacking a neuropeptide Y receptor", NATURE, 409(6819), 2001, pp. 513-517

Abstract

Neuropeptide Y (NPY) is believed to exert antinociceptive actions by inhibiting the release of substance P and other 'pain neurotransmitters' in the spinal cord dorsal horn(1-3). However, the physiological significance and potential therapeutic value of NPY remain obscure(4). It is also unclear which receptor subtype(s) are involved. To identify a possible physiological role for the NPY Y1 receptor in pain transmission, we generated NPY Y1 receptor null mutant (Y1(-/-)) mice by homologous recombination techniques. Herewe show that Y1(-/-) mice develop hyperalgesia to acute thermal, cutaneousand visceral chemical pain, and exhibit mechanical hypersensitivity. Neuropathic pain is increased, and the mice show a complete absence of the pharmacological analgesic effects of NPY. In the periphery, Y1 receptor activation is sufficient and required for substance P release and the subsequent development of neurogenic inflammation and plasma leakage. We conclude that the Y1 receptor is required for central physiological and pharmacological NPY-induced analgesia and that its activation is both sufficient and requiredfor the release of substance P and initiation of neurogenic inflammation.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 30/11/20 alle ore 03:23:58